Here are three such new findings related to the major neurocognitive concerns facing much of the rapidly ageing populations.
1. Drugs for Parkinson’s may lead to addictive behavioursThere is growing evidence that the current drugs used to manage symptoms of Parkinson’s disease, caused by low dopamine levels, have been found to lead to poor impulse control in a small number of patients. Dopamine agonists, which mimic the effect of dopamine, are among the drug treatments that can cause poor impulse control as a side effect.
Poor impulse control would subsequently lead to addictive behaviours, for example, shopping, gambling, hypersexuality that can be deviant, or even criminal, in some cases. The potentially adverse effects, such behavioural change, may impact the patient’s interpersonal relations and financial security.
Studies suggest that around 5% to 10% of those taking common drugs have an impulse control disorder.
The NHS will release a new set of guidelines specifying that the families of Parkinson’s sufferers should be warned of such side effects, and that patients should be made aware of their own behavioural changes at review appointments.
"The key thing is to make sure that the relative or other half is informed, as the people themselves actually quite enjoy it so they don't see it as a problem," said Professor Richard Walker, a consultant physician who is one of the four who contributed to the new guidelines.
2. Antioxidants do not prevent dementiaOxidative stress, the accumulation of harmful free radicals in the body, has been shown to play a pivotal role in neurodegenerative disorders such as Alzheimer’s and dementia. Hence, the idea of increasing antioxidant intake to balance the effects of oxidative stress and ameliorate cognitive impairment has been put forth. However, this has been disproved by a new study, which ran from September 2009 to May 2015.
The cohort study which was part of a clinical trial on prostate cancer, investigated the progression of dementia in 3,786 men aged 60 and above, who were randomly assigned to take vitamin E, selenium, a combination of the two, or a placebo.
Having adjusted for demographic and health factors such as race and comorbidities, the researchers concluded, “The supplemental use of vitamin E and selenium did not forestall dementia and are not recommended as preventive agents.”
“This conclusion is tempered by the underpowered study, inclusion of only men, a short supplement exposure time, dosage considerations and methodologic limitations in relying on real-world reporting of incident cases.”
3. New genetic test reveals Alzheimer’s disease onsetThe current genetic testing for Alzheimer’s focused on looking for defects in the APOE gene, which represents a 15-fold increase in risk of the disease.
A new genetic test goes a step further, calculating the age that a person is likely to develop Alzheimer’s disease. The test, which uses DNA from blood or saliva, checks for mutations in 26 genes which have been found in more than 70,000 Alzheimer’s patients.
These mutations can then be used to compute an individual’s “hazard score”. Even in people without the APOE gene defect, those with the highest hazard scores can expect to develop Alzheimer’s by the age of 84, which is 10 years earlier than those who test low.
"Equally important, testing of Alzheimer’s genetic risk can better inform prevention and therapeutic trials and be useful in determining which individuals are most likely to respond to therapy," said the study’s senior author Dr Anders Dale of the University of California San Diego School of Medicine.
Dr James Pickett, head of research at the Alzheimer’s Society, concurs but notes that the approach would have to be “tested further in mixed, non-US populations”.
Dr Rosa Sancho, head of research at Alzheimer’s Research UK, added, “This study does not suggest that having a high polygenic hazard score means you will definitely develop Alzheimer’s, nor does a low score mean you are immune from the disease. Genetics is only part of the story.” MIMS
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